This document provides an overview of shock and its management. It defines shock as an acute medical condition associated with a fall in blood pressure caused by events such as blood loss, burns, allergic reactions or sudden emotional stress. The causes of shock are discussed as cardiogenic, hypovolemic, neurogenic, anaphylactic and septic. Signs and symptoms and classification of hemorrhage are outlined. General management principles like airway maintenance, oxygen administration, IV fluids and blood transfusion are described. Surgical and local methods of hemorrhage control are also summarized. Finally, the spectrum of infections from bacteremia to septic shock and MODS as well as the treatment approach of antibiotics, source control
Simple medical student presentation about distributive shock, type and pathophysiology of each septic shock, anaphylactic shock, neurogenic shock
including management, prognosis and disposition of patient..
brief info of type of inotropes and when to start.
a clinical syndrome that results from inadequate tissue perfusion.
Hypovolemic shock - Blood or fluid loss, both leading to a decreased circulating blood volume, diastolic filling pressure, and volume.
Cardiogenic shock - due to cardiac pump failure related to loss of myocardial contractility/functional myocardium or structural/mechanical failure of the cardiac anatomy and characterized by elevations of diastolic filling pressures and volumes
Extra-cardiac/obstructive shock - due to obstruction to flow in the cardiovascular circuit and characterized by either impairment of diastolic filling or excessive afterload
Distributive shock - caused by loss of vasomotor control resulting in arteriolar/venular dilatation leading to a decrease in preload, with decreased, normal, or elevated cardiac output, depending on the presence of myocardial depression.
Simple medical student presentation about distributive shock, type and pathophysiology of each septic shock, anaphylactic shock, neurogenic shock
including management, prognosis and disposition of patient..
brief info of type of inotropes and when to start.
a clinical syndrome that results from inadequate tissue perfusion.
Hypovolemic shock - Blood or fluid loss, both leading to a decreased circulating blood volume, diastolic filling pressure, and volume.
Cardiogenic shock - due to cardiac pump failure related to loss of myocardial contractility/functional myocardium or structural/mechanical failure of the cardiac anatomy and characterized by elevations of diastolic filling pressures and volumes
Extra-cardiac/obstructive shock - due to obstruction to flow in the cardiovascular circuit and characterized by either impairment of diastolic filling or excessive afterload
Distributive shock - caused by loss of vasomotor control resulting in arteriolar/venular dilatation leading to a decrease in preload, with decreased, normal, or elevated cardiac output, depending on the presence of myocardial depression.
30 elementary, middle, and high school students came together to animate their ideas in front of a live audience in a series of short and inspiring talks. The concept of the Nspire Talks is a charity event to give kids the stage and microphone to add their voice to the collective conversation and inspire others. Speeches are no more than five minutes and cover a wide range of topics. All talks answered the question: "What's your vision for ...?"
This year's event benefitted the Michigan Eye Bank and raised awareness of the impact of the Organ Donor Registry.
د/باسم السيد
Management of shocked patient
المحاضرة التي قدمت يوم الثلاثاء 8 ابريل 2014 في دار الحكمة بالقاهرة
من فعاليات مشروع اعداد طبيب حكيم ناجح بالتعاون مع معتمد باتحاد الاطباء العرب
و ضمن موديول الطوارئ و التخدير و العناية المركزة
Shock is a life-threatening condition that occurs when the body is not getting enough blood flow. Lack of blood flow means the cells and organs do not get enough oxygen and nutrients to function properly. Many organs can be damaged as a result.
A very narrative discussion over Shock & Haemorrhage, Blood Transfusion, Blood Products which is presented in seminers. A concise guideline of a vast chapter.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
2. Shock and Management:
Presented By:
Dr. Sudhir. K. Jain, M.S, MBA(HCA), FRCS, FICS, FIAS.
Professor of Surgery,
Maulana Azad Medical College and Associated Lok Nayak Hospital,
New Delhi.
With Credits to:
Dr. Vishnuraja, PG2, Dept of Surgery, MAMC.
Dr. Ronal Kori, PG2, Dept of Surgery, MAMC.
3. Shock-(Noun)-Oxford English Dictionary
1. Sudden upsetting or surprising event or experience
2. Feeling of disturbed surprise resulting from a sudden upsetting
event
3. A disturbance causing instability in an economy
4. Short form for Electric shock
5. A violent shaking movement caused by an impact, explosion or
tremor
6. An acute medical condition associated with fall of BP caused by
events such as loss of blood, burns, allergic reactions or sudden
emotional stress.
4. Shock
Acute clinical state characterized by inadequate cellular perfusion
leading to cellular damage and failure of major organ systems.
Basic pathology is inadequate (Not always low) cardiac output for the
metabolic needs of the tissue.
6. Peripheral failure of venous return:
• True hypovolemia: Loss of blood (Ext or int hemorrhage), loss of
plasma (Burns), loss of ECF volume
• Pooling of blood (Apparent hypovolemia): Neurogenic (Spinal injury,
vasovagal attack), Anaphylactic (Ag/Ab reaction-drug allergy), Sepsis
(Endotoxic shock)
7. Signs and Symptoms
• Restless, anxious, confused and thirsty
• Cold sweating
• Cyanosed with a rapid feeble pulse
• Hypotensive
• Low urine output
• Hyperventilating
8. Signs-Contd
• CVP decreased (But in Cardiogenic shock patient have increased CVP)
• Heart rate increased, but in cardiogenic shock, HR is normal or
decreased
• PAW(v)P decreased in hypovolemic shock but increased in cardiogenic
shock
• Cardiac output decreased but in early stages of septicemic shock. It
can be increased due to hyperdynamic circulation.
9. General Measures:
• Maintain ABC-Airway, Breathing and Circulation
• Airway maintainance:
• Remove any debris, foreign body from oral cavity, throat.
• Prevent tongue from falling backward by chin lift/Jaw thrust
• If patient not able to maintain airway consider
intubation/tracheostomy.
10. Maintain Breathing:
• Give 100% oxygen
• Breathing effort inadequate
• Artificial respiration
• -Mouth to mouth breathing
• -Respiratory bag after intubation
• -Mechanical ventilator
11. Maintain Circulation:
• Control obvious haemorrhage
• Insert two large bore IV cannula
• Take blood for grouping, cross
matching
• Start IV infusion
-Normal saline/Ringer lactate
-Plantar expanders-Dextran 70, Haemacel,
Hydroxyethyl starch.
-Whole blood in moderate to severe
blood loss to maintain Hb >10 gms%
and hematocrit >30%.
12. Haemorrhage-Classification
• Depending upon nature of blood vessels
• Arterial:
Bright red colour. It jets out, pulsatile.
Pulsation of artery can be seen.
Can be easily controlled as vessel is
visible
• Venous:
Dark red in colour.
Non pulsatile, never jets out but
oozes out.
Difficult to control as vein gets
retracted.
• Capillary: Red colour, slow ooze.
13. Haemorrhage-Classification
Depending upon time of haemorrhage:
1. Primary: at the time of surgery
2. Reactionary: 6-12 hr after surgery
• Cause: Hypertension in post op period, sneezing, coughing,
retching.
3. Secondary: 5-7 days after surgery.
• Cause:Due to infection- Sloughing of vessel wall.
14. Haemorrhage-Classification
Depending upon duration of haemorrhage:
1. Acute haemorrhage: Occurs suddenly eg. Oesophageal varices
bleed
2. Chronic haemorrhage: Slow blood over long period eg. Piles,
Chronic duodenal bleed
Depending upon nature of bleeding:
1. External or revealed haemorrhage Eg.Epistaxis, haematemesis
2. Internal or concealed haemorrhage. Eg. Splenic rupture, Rupture
ectopic pregnancy.
15. Stages of Haemorrhage:
• Mild haemorrhage (Class I) <15% of blood loss (<750 cc in 70 kg man)
• Moderate (Class II) 15-30% of blood loss. Tachycardia >100. BP- Normal or
slightly increased. Anxious patient. Respiratory rate increased 20-30.
Urine output decreased 20-30 ml/hr.
• Severe (Class III) 30-40% of blood loss. HR>120 mt. BP-Decreased.
Respiratory rate increased 30-40/mt. Urine output 5-15 ml/hr. Anxious
patient, confused.
• Class VI: >40%. Patient confused and lethargics, No urine output. RR >35
• 50% loss of blood volume: Patient unconscious, BP not recordable,
Peripheral pulses not
16.
17. Treatment:
• Upto one litre < 20% of blood volume
Use of blood as replacement not required.
Crystalloids alone or crystalloids and colloid (2:1) are transfused.
If crystalloids alone used-3/4 times the blood loss volume need to be
transfused because crystalloids go into whole ECF compartment.
• 1-2 litres of blood loss (20-40%)
1 litre crystalloid (NCL 0.9%) (30-60/mt)
1 litre colloid (Dextran or haemacel)
2 redcell concentrate to restore oxygen carrying capacity.
• > 40%
Whole blood transfusion.
4.5% albumin infusion.
18. Haemorrhage Control-Local methods
• Pressure and packing
• Position and rest. Eg. Limb elevation
• Tourniquets- Pneumatic, Rubber bandage
• Contraindication- Venous haemorrhage, Pt with peripheral vascular
disease
20. Spectrum of Infections:
There exists a spectrum of disease starting with bacteria leading to
Septic Shock and MODS
• Bacteremia: Presence of bacteria in the blood (Can be natural during
straining/defaecation)
• Septicemia: Presence of microbes or toxins in blood (Pathological)
• SIRS: Systemic inflammatory response syndrome:
Diagnostic Criteria: if two or more of the following present.
21. SIRS: Diagnostic Criteria
Two or more of the following:
• Temperature >38 degree or <36 degree
• Heart rate > 90/min
• Respiratory rate > 20/min or partial pressure of carbon dioxide in
arterial blood PaCO2 of less than 32 mm Hg.
• Leukocytosis (WBC > 12000/mm3) or Leukopenia (WBC <4000/mm3)
22. Spectrum of Septic Shock:
• Sepsis: Confirmed infection and atleast two SIRS criteria
• Severe sepsis: Sepsis and organ dysfunction as evidenced by arterial
hypoxemia, lactic acidosis, oliguria, altered mental status and so on.
• Septic Shock: Sepsis and hypotension refractory to fluid
resuscitation
23. Septic shock: Mechanism
• Nitric oxide and Prostacyclin and inflammatory
mediators produced during Septic shock cause
Vasodilation, leads to hypoperfusion
• Inflammatory mediators also cause Capillary
thrombosis, leukocyte plugging of Capillaries.
• Tissue hypoperfusion, Capillary thrombosis and
leukocyte plugging in organs leads to ORGAN
FAILURE
24. Septic Shock-Treatment
• Antibiotics- to control infection
• Removal of Source of infection- Eg: Abscess drainage, Removal of
infected catheters etc.
• Hemodynamic, metabolic and respiratory support.
25. Septic Shock-Goal directed Therapy:
Goals:
1. Mean arterial pressure > 65 mm Hg
2. Saturation of Central venous oxygen (ScvO2
>70%)
Method:
Give CVP guided fluids
If MAP less than 65 mm Hg, Start Ionotropes
If MAP more than 65 mm Hg, look for ScvO2
If ScvO2 less than 70%, Start Ionotropes
If ScvO2 more than 70%, Observe